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What is Magnesium L-Threonate?
Researchers suggest that Magnesium L-Threonate could revolutionize the field of mental nourishment and help everyone achieve and maintain optimum cognitive function at every stage of life.
Thankfully, researchers at MIT discovered that Magnesium L-Threonate is able to maximize the amount of magnesium your brain can absorb . Not only that, researchers noted Magnesium L-Threonate improved both short term and long term memory
In preliminary research published in the prestigious journal Neuron in 2010, MIT researchers screened every available form of supplemental magnesium and demonstrated in an animal model that Magnesium L-Threonate—and only Magnesium L-Threonate—has the ability to cross into the brain and boost magnesium levels. In their experiments, this increase in brain magnesium concentrations resulted in observable benefits in key cognitive measures.How does Magnesium L-Threonate work?
By boosting magnesium levels within the brain, scientists believe Magnesium L-Threonate helps neurons maintain a state of healthy sustained activity—neither over-stimulated nor under-stimulated. One could say that Magnesium L-Threonate helps keep the brain firing on all cylinders. And, scientists believe, by maintaining this healthy homeostasis, the brain can more easily respond to mental demands and perform cognitive tasks with less stress and fatigue.Benefits of taking Magnesium L-Threonate supplements:1.Magnesium L-threonate for learning and memory>Enhancement of learning and memory by elevating brain magnesium.
Slutsky I1, Abumaria N, Wu LJ, Huang C, Zhang L, Li B, Zhao X, Govindarajan A, Zhao MG, Zhuo M, Tonegawa S, Liu G.
Author information
Abstract
Learning and memory are fundamental brain functions affected by dietary and environmental factors. Here, we show that increasing brain magnesium using a newly developed magnesium compound (magnesium-L-threonate, MgT) leads to the enhancement of learning abilities, working memory, and short- and long-term memory in rats. The pattern completion ability was also improved in aged rats. MgT-treated rats had higher density of synaptophysin-/synaptobrevin-positive puncta in DG and CA1 subregions of hippocampus that were correlated with memory improvement. Functionally, magnesium increased the number of functional presynaptic release sites, while it reduced their release probability. The resultant synaptic reconfiguration enabled selective enhancement of synaptic transmission for burst inputs. Coupled with concurrent upregulation of NR2B-containing NMDA receptors and its downstream signaling, synaptic plasticity induced by correlated inputs was enhanced. Our findings suggest that an increase in brain magnesium enhances both short-term synaptic facilitation and long-term potentiation and improves learning and memory functions.>Magnesium L-threonate prevents and restores memory deficits associated with neuropathic pain by inhibition of TNF-α.
Wang J1, Liu Y, Zhou LJ, Wu Y, Li F, Shen KF, Pang RP, Wei XH, Li YY, Liu XG.
Author information
Abstract
BACKGROUND:
Clinical studies have shown that about two-thirds of patients with chronic pain suffer from short-term memory (STM) deficits and an effective drug for treatment of the neurological disorder is lacking at present.
OBJECTIVE:
We tested whether chronic oral application of magnesium L-threonate (MgT), which has been shown to improve memory in normal and aging animals by elevating Mg2+ in the brain, could prevent or restore the STM deficits induced by spared nerve injury (SNI), an animal model of chronic neuropathic pain. The mechanisms underlying the effect of MgT on STM deficits were also investigated.
STUDY DESIGN:
The experiments were conducted in a random and double-blind fashion in adult male rats. MgT was administrated via drinking water at a dose of 609 mg/kg/d for 2 weeks, starting either one week before SNI (preventative group) or one week after SNI (therapeutic group), and water without the drug served as control.
METHODS:
STM was accessed with a novel object recognition test (NORT), followed by recording of long-term potentiation (LTP) in the hippocampus in vivo and the measurement of the expression of tumor necrosis factor-α (TNF-α) with Western Blot or Immunohistochemistrical staining, a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor (NMDAR) currents were recorded with patch clamp in CA1 neurons in acute and cultured hippocampal slices.
RESULT:
We found that chronic oral application of MgT was able to prevent and restore the deficits of STM and of LTP at CA3-CA1 synapses in the hippocampus induced by SNI. Furthermore, both preventative and therapeutic chronic oral application of MgT blocked the up-regulation of TNF-α in the hippocampus, which has been previously shown to be critical for memory deficits. SNI reduced NMDAR current and the effect was dramatically attenuated by elevating extracellular Mg2+ concentration ([Mg2+]○). In cultured hippocampal slices, chronic application of recombinant rat TNF-α (rrTNF-α) for 3 days reduced NMDAR current in a concentration-dependent manner and the effect was again blocked by elevating [Mg2+]○.
LIMITATIONS:
We showed that oral application of MgT inhibited the over-expression of TNF-α and rescued the dysfunction of the NMDAR, but the causal relationship between them remains elusive.
CONCLUSIONS:
Our data suggested that oral application of MgT was able to prevent and restore the STM deficits in an animal model of chronic neuropathic pain by reversing the dysfunction of the NMDAR, and normalization of TNF-α expression may play a role in the effect. Oral application of MgT may be a simple and potent means for handling this form of memory deficit.>Targeting the NMDA receptor subunit NR2B for treating or preventing age-related memory decline.
Wang D1, Jacobs SA, Tsien JZ.
Author information
1Banna Biomedical Research Institute , Xishuangbanna, Yunnan , China.
Abstract
INTRODUCTION:
Age-related memory loss is believed to be a result of reduced synaptic plasticity, including changes in the NR2 subunit composition of the NMDA receptor. It is known that endogenous NR2B subunits decrease as the brain ages, whereas transgenic upregulation of NR2B enhances synaptic plasticity and learning and memory in several animal species. Accumulating evidence suggests that elevated brain magnesium levels, via dietary supplementation, can boost NR2B in the brain, consequently reversing memory deficits and enhancing cognitive abilities.
AREAS COVERED:
This review highlights the convergent molecular mechanisms via the NR2B pathway as a useful strategy for treating age-related memory loss. A dietary approach, via oral intake of a novel compound, magnesium L-threonate (MgT), to boost NR2B expression in the brain is highlighted.
EXPERT OPINION:
Direct upregulation of the NR2B subunit expression can enhance synaptic plasticity and memory functions in a broad range of behavioral tasks in rodents. Other upregulation approaches, such as targeting the NR2B transporter or surface recycling pathway via cyclin-dependent kinase 5, are highly effective in improving memory functions. A dietary supplemental approach by optimally elevating the [Mg²⁺] in the brain is surprisingly effective in upregulating NR2B expression and improving memories in preclinical studies. MgT is currently under clinical trials.>Efficacy and Safety of MMFS-01, a Synapse Density Enhancer, for Treating Cognitive Impairment in Elderly: A Randomized, Double-Blind, Placebo-Controlled Trial.
Liu G1,2, Weinger JG1, Lu ZL3, Xue F4, Sadeghpour S1.
Author information
1Neurocentria, Inc., Fremont, CA, USA.
2School of Medicine, Tsinghua University, Beijing, China.
3Department of Psychology, The Ohio State University, Columbus, OH, USA.
4Department of Psychology, University of Southern California, Los Angeles, CA, USA.
Abstract
BACKGROUND:
Cognitive impairment is a major problem in elderly, affecting quality of life. Pre-clinical studies show that MMFS-01, a synapse density enhancer, is effective at reversing cognitive decline in aging rodents.
OBJECTIVE:
Since brain atrophy during aging is strongly associated with both cognitive decline and sleep disorder, we evaluated the efficacy of MMFS-01 in its ability to reverse cognitive impairment and improve sleep.
METHODS:
We conducted a randomized, double-blind, placebo-controlled, parallel-designed trial in elderly subjects (age 50-70) with cognitive impairment. Subjects were treated with MMFS-01 (n = 23) or placebo (n = 21) for 12 weeks and cognitive ability, sleep quality, and emotion were evaluated. Overall cognitive ability was determined by a composite score of tests in four major cognitive domains.
RESULTS:
With MMFS-01 treatment, overall cognitive ability improved significantly relative to placebo (p = 0.003; Cohen’s d = 0.91). Cognitive fluctuation was also reduced. The study population had more severe executive function deficits than age-matched controls from normative data and MMFS-01 treatment nearly restored their impaired executive function, demonstrating that MMFS-01 may be clinically significant. Due to the strong placebo effects on sleep and anxiety, the effects of MMFS-01 on sleep and anxiety could not be determined.
CONCLUSIONS:
The current study demonstrates the potential of MMFS-01 for treating cognitive impairment in elderly.2.Magnesium L-Threonate and Alzheimer’s disease>Elevation of brain magnesium prevents and reverses cognitive deficits and synaptic loss in Alzheimer’s disease mouse model.
Li W1, Yu J, Liu Y, Huang X, Abumaria N, Zhu Y, Huang X, Xiong W, Ren C, Liu XG, Chui D, Liu G.
Author information
Retraction in
Author-initiated retraction: Li et al., Elevation of brain magnesium prevents and reverses cognitive deficits and synaptic loss in Alzheimer’s disease mouse model. [J Neurosci. 2014]
Abstract
Profound synapse loss is one of the major pathological hallmarks associated with Alzheimer’s disease (AD) and might underlie memory impairment. Our previous work demonstrated that the magnesium ion is a critical factor in controlling synapse density/plasticity. Here, we investigated whether elevation of brain magnesium by the use of a recently developed compound, magnesium-l-threonate (MgT), can ameliorate the AD-like pathologies and cognitive deficits in the APPswe/PS1dE9 mice, a transgenic (Tg) mouse model of AD. MgT treatment reduced Aβ plaque and prevented synapse loss and memory decline in the Tg mice. Strikingly, MgT treatment was effective even when given to the mice at the end stage of their AD-like pathological progression. To explore how elevation of brain magnesium ameliorates the AD-like pathologies in the brains of Tg mice, we studied molecules critical for APP metabolism and signaling pathways implicated in synaptic plasticity/density. In the Tg mice, the NMDAR/CREB/BDNF signaling was downregulated, whereas calpain/calcineurin/Cdk5 neurodegenerative signaling and β-secretase (BACE1) expression were upregulated. MgT treatment prevented the impairment of these signaling pathways, stabilized BACE1 expression, and reduced soluble APPβ and β-C-terminal fragments in the Tg mice. At the molecular level, elevation of extracellular magnesium prevented the high-Aβ-induced reductions in synaptic NMDARs by preventing calcineurin overactivation in hippocampal slices. Correlation studies suggested that the protection of NMDAR signaling might underlie the stabilization of BACE1 expression. Our results suggest that elevation of brain magnesium exerts substantial synaptoprotective effects in a mouse model of AD and may have therapeutic potential for treating AD in humans.>By suppressing the expression of anterior pharynx-defective-1α and -1β and inhibiting the aggregation of β-amyloid protein, magnesium ions inhibit the cognitive decline of amyloid precursor protein/presenilin 1 transgenic mice.
Yu X1, Guan PP1, Guo JW1, Wang Y1, Cao LL1, Xu GB1, Konstantopoulos K1, Wang ZY2, Wang P2.
Author information
Abstract
Alzheimer’s disease (AD) is associated with a magnesium ion (Mg2+) deficit in the serum or brain. However, the mechanisms regulating the roles of Mg2+ in the pathologic condition of AD remain unknown. We studied whether brain Mg2+ can decrease β-amyloid (Aβ) deposition and ameliorate the cognitive decline in a model of AD, the APPswe/PS1DE9 transgenic (Tg) mouse. We used a recently developed compound, magnesium-l-threonate (MgT), for a treatment that resulted in enhanced clearance of Aβ in an anterior pharynx-defective (APH)-1α/-1β-dependent manner. To further explore how MgT treatment inhibits cognitive decline in APP/PS1 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling pathways were investigated. In neurons, ERK1/2 and PPARγ signaling pathways were activated by MgT treatment, which in turn suppressed (by >80%) the expression of APH-1α/-1β, which is responsible for the deposition of Aβ and potentially contributes to the memory deficit that occurs in AD. More important, Aβ oligomers in the cerebrospinal fluid (CSF) further promoted the expression of APH-1α/-1β (by >2.5-fold), which enhances the γ-cleavage of APP and Aβ deposition during AD progression. These findings provide new insights into the mechanisms of AD progression and are instrumental for developing better strategies to combat the disease.-Yu, X., Guan, P.-P., Guo, J.-W., Wang, Y., Cao, L.-L., Xu, G.-B., Konstantopoulos, K., Wang, Z.-Y., Wang, P. By suppressing the expression of anterior pharynx-defective-1α and -1β and inhibiting the aggregation of β-amyloid protein, magnesium ions inhibit the cognitive decline of amyloid precursor protein/presenilin 1 transgenic mice.3.Magnesium L-threonate and memory>Magnesium L-threonate prevents and restores memory deficits associated with neuropathic pain by inhibition of TNF-α.
Wang J1, Liu Y, Zhou LJ, Wu Y, Li F, Shen KF, Pang RP, Wei XH, Li YY, Liu XG.
Author information
Abstract
BACKGROUND:
Clinical studies have shown that about two-thirds of patients with chronic pain suffer from short-term memory (STM) deficits and an effective drug for treatment of the neurological disorder is lacking at present.
OBJECTIVE:
We tested whether chronic oral application of magnesium L-threonate (MgT), which has been shown to improve memory in normal and aging animals by elevating Mg2+ in the brain, could prevent or restore the STM deficits induced by spared nerve injury (SNI), an animal model of chronic neuropathic pain. The mechanisms underlying the effect of MgT on STM deficits were also investigated.
STUDY DESIGN:
The experiments were conducted in a random and double-blind fashion in adult male rats. MgT was administrated via drinking water at a dose of 609 mg/kg/d for 2 weeks, starting either one week before SNI (preventative group) or one week after SNI (therapeutic group), and water without the drug served as control.
METHODS:
STM was accessed with a novel object recognition test (NORT), followed by recording of long-term potentiation (LTP) in the hippocampus in vivo and the measurement of the expression of tumor necrosis factor-α (TNF-α) with Western Blot or Immunohistochemistrical staining, a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor (NMDAR) currents were recorded with patch clamp in CA1 neurons in acute and cultured hippocampal slices.
RESULT:
We found that chronic oral application of MgT was able to prevent and restore the deficits of STM and of LTP at CA3-CA1 synapses in the hippocampus induced by SNI. Furthermore, both preventative and therapeutic chronic oral application of MgT blocked the up-regulation of TNF-α in the hippocampus, which has been previously shown to be critical for memory deficits. SNI reduced NMDAR current and the effect was dramatically attenuated by elevating extracellular Mg2+ concentration ([Mg2+]○). In cultured hippocampal slices, chronic application of recombinant rat TNF-α (rrTNF-α) for 3 days reduced NMDAR current in a concentration-dependent manner and the effect was again blocked by elevating [Mg2+]○.
LIMITATIONS:
We showed that oral application of MgT inhibited the over-expression of TNF-α and rescued the dysfunction of the NMDAR, but the causal relationship between them remains elusive.
CONCLUSIONS:
Our data suggested that oral application of MgT was able to prevent and restore the STM deficits in an animal model of chronic neuropathic pain by reversing the dysfunction of the NMDAR, and normalization of TNF-α expression may play a role in the effect. Oral application of MgT may be a simple and potent means for handling this form of memory deficit.4.Magnesium L-Threonate and fear>Effects of elevation of brain magnesium on fear conditioning, fear extinction, and synaptic plasticity in the infralimbic prefrontal cortex and lateral amygdala.
Abumaria N1, Yin B, Zhang L, Li XY, Chen T, Descalzi G, Zhao L, Ahn M, Luo L, Ran C, Zhuo M, Liu G.
Author information
Abstract
Anxiety disorders, such as phobias and posttraumatic stress disorder, are among the most common mental disorders. Cognitive therapy helps in treating these disorders; however, many cases relapse or resist the therapy, which justifies the search for cognitive enhancers that might augment the efficacy of cognitive therapy. Studies suggest that enhancement of plasticity in certain brain regions such as the prefrontal cortex (PFC) and/or hippocampus might enhance the efficacy of cognitive therapy. We found that elevation of brain magnesium, by a novel magnesium compound [magnesium-l-threonate (MgT)], enhances synaptic plasticity in the hippocampus and learning and memory in rats. Here, we show that MgT treatment enhances retention of the extinction of fear memory, without enhancing, impairing, or erasing the original fear memory. We then explored the molecular basis of the effects of MgT treatment on fear memory and extinction. In intact animals, elevation of brain magnesium increased NMDA receptors (NMDARs) signaling, BDNF expression, density of presynaptic puncta, and synaptic plasticity in the PFC but, interestingly, not in the basolateral amygdala. In vitro, elevation of extracellular magnesium concentration increased synaptic NMDAR current and plasticity in the infralimbic PFC, but not in the lateral amygdala, suggesting a difference in their sensitivity to elevation of brain magnesium. The current study suggests that elevation of brain magnesium might be a novel approach for enhancing synaptic plasticity in a regional-specific manner leading to enhancing the efficacy of extinction without enhancing or impairing fear memory formation.>Magnesium supplement enhances spatial-context pattern separation and prevents fear overgeneralization.
Abumaria N1, Luo L, Ahn M, Liu G.
Author information
Abstract
Enhancement of pattern separation could be helpful in improving the quality of normal daily learning and in treating individuals with cognitive impairment and certain psychiatric disorders. Previously, we have shown that elevating brain magnesium, by a novel magnesium compound (magnesium-L-threonate; MgT), enhances extinction of fear memory without enhancing amygdala-dependent fear memory. Here, we investigated the effects of MgT treatment on contextual-fear memory and subsequent pattern separation. Sprague-Dawley male rats were treated with MgT for 4 weeks and memory was evaluated using a spatial-context fear conditioning task. The pattern separation ability of MgT-treated rats was assessed using a spatial-context-discrimination task. MgT treatment did not enhance the retention of contextual-fear memory. Interestingly, the ability to discriminate between two, more or less distinct, contexts was enhanced in MgT-treated rats. Our results suggest that elevation of brain magnesium might be helpful in enhancing spatial-context discrimination and/or pattern separation besides preventing aversive-event-induced overgeneralization of fear.Side effects and safety of Magnesium L-Threonate
The intestinal absorption of magnesium varies depending on how much magnesium the body needs, so there are not very many side-effects associated with supplementation. If there is too much magnesium, the body will only absorb as much as it needs. However, excessive doses may cause gastrointestinal distress and diarrhea.
There have been no side effects reported.Dosage of Magnesium L-Threonate supplement:
The recommended dietary allowance for magnesium for adults 19-30 years old is 400 milligrams/day for men and 310 milligrams/day for non-pregnant women. For adults 31 and older, it is 420 milligrams/day for men and 320 milligrams/day for non-pregnant women.
The improvement of cognition and memory , Recommended for commonly 1-2g/day.